The absence of FOXP1 and FOXP4 in Tregs leads to an intact compartment but with Tregs expressing lower levels of CD25 on a per-cell basis, suggesting that the AIHA phenotype and subsequent early lethality arise from Treg-intrinsic functional defects related to attenuated IL-2/IL-2R signaling. Here, FOXP4 is linked to autoimmune hemolytic anemia.